PMID- 17008059
OWN - NLM
STAT- MEDLINE
DCOM- 20061221
LR  - 20131121
IS  - 0923-1811 (Print)
IS  - 0923-1811 (Linking)
VI  - 44
IP  - 2
DP  - 2006 Nov
TI  - Macrophage-derived chemokine (MDC)/CCL22 produced by monocyte derived dendritic 
      cells reflects the disease activity in patients with atopic dermatitis.
PG  - 93-9
AB  - BACKGROUND: Atopic dermatitis (AD) is a recurrent inflammatory skin disease 
      characterized by high serum levels of IgE and Th2-type cytokines such as IL-4, 
      IL-5 or IL-13. Chemokines attract leukocytes in inflamed tissues. We have 
      previously found that thymus and activation regulated chemokine (TARC)/CCL17 and 
      macrophage-derived chemokine (MDC)/CCL22 are highly secreted in the plasma levels 
      of AD patients. Dendritic cells (DCs) are antigen-presenting cells that are 
      divided into two subgroups including monocyte derived DCs (MoDCs) and 
      plasmacytoid DCs (pDCs). OBJECTIVES: The aim of the study was to elucidate CCL17 
      and CCL22 production by MoDCs in AD patients, psoriasis vulgaris (PsV) patients 
      and healthy controls (HC). METHODS: MoDCs were obtained from AD patients, PsV 
      patients or HC and were cultured. In addition, the chemokine levels were measured 
      in the supernatants. RESULTS: We found that the CCL22 levels produced by MoDCs in 
      AD patients to be significantly higher than those of PsV patients and HC. There 
      was a significant correlation between the CCL22 levels produced by MoDCs and the 
      SCORAD index. No significant difference in the CCL17 levels produced by MoDCs was 
      detected among AD patients, PsV patients or HC. Immunosuppressive drugs such as 
      dexamethasone (Dex), tacrolimus and cyclosporine (Cys) inhibited the CCL22 
      production by MoDCs in the AD patients. CONCLUSION: These data suggest that the 
      CCL22 level produced by MoDCs thus reflects the disease activity of AD and it may 
      also play an important role regarding the production of CCL22 in the pathogenesis 
      of AD.
FAU - Hashimoto, Shinichi
AU  - Hashimoto S
AD  - Department of Dermatology, Fukushima Medical University, Hikarigaoka-1, 
      Fukushima, Fukushima 960-1295, Japan.
FAU - Nakamura, Koichiro
AU  - Nakamura K
FAU - Oyama, Noritaka
AU  - Oyama N
FAU - Kaneko, Fumio
AU  - Kaneko F
FAU - Tsunemi, Yuichiro
AU  - Tsunemi Y
FAU - Saeki, Hidehisa
AU  - Saeki H
FAU - Tamaki, Kunihiko
AU  - Tamaki K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20060927
PL  - Netherlands
TA  - J Dermatol Sci
JT  - Journal of dermatological science
JID - 9011485
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (CCL17 protein, human)
RN  - 0 (CCL22 protein, human)
RN  - 0 (Chemokine CCL17)
RN  - 0 (Chemokine CCL22)
RN  - 0 (Chemokines, CC)
RN  - 0 (Dermatologic Agents)
RN  - 0 (Immunosuppressive Agents)
RN  - 0 (Interleukin-18)
RN  - 187348-17-0 (Interleukin-12)
RN  - 7S5I7G3JQL (Dexamethasone)
RN  - 83HN0GTJ6D (Cyclosporine)
RN  - WM0HAQ4WNM (Tacrolimus)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Anti-Inflammatory Agents/pharmacology
MH  - Chemokine CCL17
MH  - Chemokine CCL22
MH  - Chemokines, CC/genetics/*metabolism
MH  - Cyclosporine/pharmacology
MH  - Dendritic Cells/drug effects/*metabolism/pathology
MH  - Dermatitis, Atopic/genetics/*metabolism/pathology
MH  - Dermatologic Agents/pharmacology
MH  - Dexamethasone/pharmacology
MH  - Female
MH  - Gene Expression Regulation/drug effects/genetics
MH  - Humans
MH  - Immunosuppressive Agents/pharmacology
MH  - Interleukin-12/genetics/metabolism
MH  - Interleukin-18/genetics/metabolism
MH  - Male
MH  - Middle Aged
MH  - Monocytes/drug effects/*metabolism/pathology
MH  - Psoriasis/genetics/metabolism/pathology
MH  - Severity of Illness Index
MH  - Tacrolimus/pharmacology
EDAT- 2006/09/30 09:00
MHDA- 2006/12/22 09:00
CRDT- 2006/09/30 09:00
PHST- 2006/03/26 00:00 [received]
PHST- 2006/07/04 00:00 [revised]
PHST- 2006/08/06 00:00 [accepted]
PHST- 2006/09/30 09:00 [pubmed]
PHST- 2006/12/22 09:00 [medline]
PHST- 2006/09/30 09:00 [entrez]
AID - S0923-1811(06)00225-8 [pii]
AID - 10.1016/j.jdermsci.2006.08.004 [doi]
PST - ppublish
SO  - J Dermatol Sci. 2006 Nov;44(2):93-9. doi: 10.1016/j.jdermsci.2006.08.004. Epub 
      2006 Sep 27.